Phosphorylation of the Acetylcholine Receptor
There is increasing evidence that disorders of recep tor function account for several major clinical diseases. In the nervous system, two of the most striking examples are myasthenia gravis and tardive dyskinesia. Each of these conditions is associated with a change in the number and/or sensitivity of a neurotransmitter receptor. In myasthenia gravis, fatigue and weakness is best explained by a decreased number of nicotinic acetylcholine receptors (AChR) at the neuromuscular junction. On the other hand, the movement disorder in tardive dyskinesia is best explained by an apparent increase in the number and sensitivity of dopamine receptors in the corpus striatum. It seems likely therefore that changes in specific biochemical mechanisms which regulate post-synaptic membrane receptor proteins account for the pathophysiologic abnormalities in each of these disorders. Such mechanisms might involve covalent biochemical modification of the receptor such as phosphorylation, methylation or acetylation, or conformational changes in the receptor as a result of its interaction with effectors. However, the biochemical regulatory mechanisms affecting receptor proteins at the synapse have not yet been identified and we do not know how these are altered in neurologic disease.
KeywordsAcetylcholine Receptor Tardive Dyskinesia Electric Organ Photoaffinity Label Enrich Membrane
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